Bronchitis by Ignacio Martín-Loeches

By Ignacio Martín-Loeches

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Extra resources for Bronchitis

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Am Rev Respir Dis 1988;137:726 - 741. [65] Puchelle E, Zahm JM, Girard F, Bertrand A, Polu JM, Aug F, Sdoul P. Mucociliary transport in vivo and in vitro. Relations to sputum properties in chronic bronchitis. Eur J Respir Dis 1980;61:254 - 264. [66] Hasania A, Pavia D. Cough as a clearance mechanism. , editor. Cough 1989;Raven Press. New York. [67] Pavia D. Lung mucociliary clearance. , editor. Aerosols and the lung 1984;Butterworths. Boston. [68] Smallman LA, Hill SL, Stockley RA. Reduction of ciliary beat frequency in vitro by sputum from patients with bronchiectasis: A serine proteinase effect.

Mortality in relation to smoking: 40 years' observations on male british doctors. BMJ 1994;309:901 - 911. [8] Tashkin DP, Clark VA, Coulson AH, Simmons M, Bourque LB, Reems C, Detels R, Sayre JW, Rokaw SN. The ucla population studies of chronic obstructive respiratory disease. Viii. Effects of smoking cessation on lung function; a prospective study of a free-living population. Am Rev Respir Dis 1984;130:707 - 715. [9] Sanford AJ, Silverman EK. 1: Susceptibility factors for copd the genotype-environment interaction.

Bacterial Killing Induces Inflammatory Cell migration Intra-cellular : bactericidal following engulfment of organisms in phagosome Extra cellular: Targeting and cleaving bacterial virulence factors in released granule proteins NE/alpha 1 antitrypsin complexes are chemotactic for neutrophils Modification of ICAM1 expression enhancing adhesion Degradation by proteolysis Degrades all components of Extracellular Matrix Degrades Cystatin C Degrades inhibitors of proteinases Cleaves T Lymphocyte surface antigen Activation of proteinases by post-transcriptional modifications Activates proteinases including MMP-2, MMP-3, MMP-9, and Cathepsin B Modification of inflammatory mediators, enhancing inflammation Enhances epithelial secretion of IL8 Enhances macrophage secretion of LTB4 Inhibits cellular response to inhibitors of inflammatory mediators, for example, TNFsR1 Prolongs the half life of inflammatory mediators including TNF Increases alpha1-AT expression by monocytes and alveolar macrophages Enhances Cell Apoptosis Increases epithelial and endothelial cell apoptosis Alteration of Cell function Disruption and detachment of epithelial cells Reduces ciliary beating of columnar epithelium Enhances oxidative stress Increases mucin production Increases bacterial adherence and colonisation on the epithelium Table 1.

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